Jeff Dangl was born on October 13, 1957, in Grand Rapids, Michigan, and grew up in northern California. He received bachelor’s degrees in biological sciences and English (modern literature) and a master’s degree in biological sciences from Stanford University in 1981. His doctoral work concerned structure-function relationships of genetically engineered chimeric monoclonal antibodies in the Genetics Department of Stanford Medical School. He finished his Ph.D. degree in 1986. In the same year, he was awarded an NSF Plant Molecular Biology Fellowship to pursue post-doctoral research at the Max Planck Institute of Plant Breeding in Cologne, Germany, in the department of Klaus Hahlbrock. In 1989, he began his own group at the Max Delbrück Laboratory, also in Cologne. In 1995, the Dangl lab moved to the University of North Carolina at Chapel Hill. He was named John N. Couch Distinguished Professor in 1999 and a Howard Hughes Medical Institute Investigator (HHMI) in 2011.
Dangl is receiving the Ruth Allen Award for his seminal and sustained contributions to the discipline of molecular plant pathology that led to a coherent definition of the plant immune system. In 1995, Dangl identified RPM1, one of the first disease resistance genes to be cloned. RPM1 is remarkable because it conditions resistance to bacterial strains expressing either of two sequence-unrelated type III effector proteins, AvrRpm1 or AvrB. These type III effectors are, to date, never found in the same bacterial strain but can confer virulence to strains expressing them. Hence, they provide redundant virulence functions without sequence similarity. RPM1 is the first example of a dual specificity disease resistance protein, a discovery with important implications for our basic understanding of plant immunity. Indeed, this finding that multiple effectors activate a single immune receptor drove subsequent thinking about “indirect recognition” of “modified self” that resulted in conceptual breakthroughs, such as the Guard Hypothesis, which Dangl and Jones first articulated in an influential Nature review (Dangl and Jones, 2001, Nature 411:826). Dangl went on to test key predictions of the Guard Hypothesis; namely, that sequence-unrelated effectors converged onto the same host target. In the first of three highly influential Cell papers (Mackey et al., 2002, Cell 108:743), Dangl’s lab demonstrated that sequence-unrelated type III effectors, AvrB and AvrRpm1, target the same plant protein RIN4. Biochemical modification of RIN4 by these effectors is the signal through which the plant immune receptor RPM1 senses bacterial invasion.
Another of Dangl’s long-term interests is the genetic control of the hypersensitive response (HR), the programmed cell death reaction that is often associated with disease resistance. Dangl and colleagues made key discoveries that resulted in a comprehensive understanding of HR regulation by plant cells. In the mid-1990s, the Dangl lab isolated some of the first mutants that mis-regulate HR cell death in the absence of pathogen. One mutant, lsd1, exhibits normal HR timing and extent but cannot control subsequent runaway cell death that consumes the leaf. This phenotype is driven by extracellular superoxide produced in response to infection by the enzyme NADPH-dependent oxidoreductase AtRbohD. The oxidative burst drives local accumulation of the plant defense hormone salicylic acid (SA) in cells surrounding infection sites to up-regulate defense and antioxidant gene transcription. This work forced an overhaul in thinking of reactive oxygen signaling during plant defense, because the loss of atrbohD dramatically enhanced the cell death phenotype. This enhancement was SA dependent. Thus, reactive oxygen generated by AtrbohD proteins can antagonize SA-dependent pro-death signals at the margins of an infection zone. The result is suppression of unwanted cell death in the face of the increasing SA levels required to initiate appropriate defense responses beyond the initial infection site.
Dangl has taken several leadership roles to service the science of plant biology and molecular plant pathology. He is a past member of the National Research Council’s Board of Life Sciences and a past member of the North American Arabidopsis Steering Committee (elected) and of the NSF Eukaryotic Genetics and NIH Genetics, Variation and Evolution Grants Panels. Dangl is currently a member of reviewing editorial boards of Science, Cell, PNAS, and PLoS Biology, and served as co-editor-in-chief of Current Opinions in Plant Biology. Dangl received several awards for his research accomplishments. He is an elected member of the U.S. National Academy of Sciences (2007) and the American Academy of Microbiology (2010). He is a fellow of the American Association for the Advancement of Science (elected, 2004). He is also an elected foreign associate of the German Academy of Sciences (Die Leoplodina, 2003). Research in the Dangl lab is funded by HHMI, NIH, NSF, and DOE. Dangl has been an inspirational figure in the field of plant-microbe interactions. His record reflects a sustained commitment to opening new, relevant, and high-risk research arenas. He authored a number of highly cited influential reviews that were often ahead of the curve in the concepts and ideas they put forward. He trained a large cohort of post-docs, doctoral, and undergraduate students, many of who are now professors in top flight research universities around the world.
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